scholarly journals Experimental Models of Acute Lung Injury: their Advantages and Limitations

2020 ◽  
Vol 20 (3) ◽  
pp. 90-102
Author(s):  
D Mokra ◽  
P Mikolka ◽  
P Kosutova ◽  
A. Calkovska
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Animal Experiments ◽  
Specific Treatment ◽  
Severe Trauma ◽  
Therapeutic Strategies ◽  
Experimental Models ◽  
Lung Protective Ventilation ◽  
Novel Therapeutic Strategies ◽  
Complex Methods

AbstractAcute damage to the lung may originate from various direct and indirect reasons. Direct lung injury may be caused by pneumonia, near-drowning, aspiration, inhalation of toxic gases etc., while indirect lung injury is secondary, following any severe extra-pulmonary disease, e.g. sepsis, acute pancreatitis, or severe trauma. Due to a complex pathophysiology of the acute lung injury, the treatment is also extremely complicated and except for lung-protective ventilation there have been no specific treatment approaches recommended. An urgent need for a reliable and sufficiently effective treatment forces the researchers into testing novel therapeutic strategies. However, most of these determinations should be done in the laboratory conditions using animals. Complex methods of preparation of various experimental models of the acute lung injury has gradually developed within decades. Nowadays, there have been the models of direct, indirect, or mixed lung injury well established, as well as the models evoked by a combination of two triggering factors. Although the applicability of the results from animal experiments to patients might be limited by many factors, animal models are essential for understanding the patho-physiology of acute lung injury and provide an exceptional opportunity to search for novel therapeutical strategies.

scholarly journals Alternative and Natural Therapies for Acute Lung Injury and Acute Respiratory Distress Syndrome

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Vipul J. Patel ◽  
Sreeja Biswas Roy ◽  
Hiren J. Mehta ◽  
Myungsoo Joo ◽  
Ruxana T. Sadikot
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Experimental Models ◽  
Lung Protective Ventilation ◽  
Related Factor ◽  
Made In

Introduction. Acute respiratory distress syndrome (ARDS) is a complex clinical syndrome characterized by acute inflammation, microvascular damage, and increased pulmonary vascular and epithelial permeability, frequently resulting in acute respiratory failure and death. Current best practice for ARDS involves “lung-protective ventilation,” which entails low tidal volumes and limiting the plateau pressures in mechanically ventilated patients. Although considerable progress has been made in understanding the pathogenesis of ARDS, little progress has been made in the development of specific therapies to combat injury and inflammation. Areas Covered. In recent years, several natural products have been studied in experimental models and have been shown to inhibit multiple inflammatory pathways associated with acute lung injury and ARDS at a molecular level. Because of the pleiotropic effects of these agents, many of them also activate antioxidant pathways through nuclear factor erythroid-related factor 2, thereby targeting multiple pathways. Several of these agents are prescribed for treatment of inflammatory conditions in the Asian subcontinent and have shown to be relatively safe. Expert Commentary. Here we review natural remedies shown to attenuate lung injury and inflammation in experimental models. Translational human studies in patients with ARDS may facilitate treatment of this devastating disease.

scholarly journals Plasma mitochondrial DNA levels are associated with acute lung injury and mortality in septic patients

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jia-yu Mao ◽  
Dong-kai Li ◽  
Hong-min Zhang ◽  
Xiao-ting Wang ◽  
Da-wei Liu
Keyword(s):  
Mitochondrial Dna ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Survival Rates ◽  
Experimental Models ◽  
College Hospital ◽  
Medical College ◽  
Incidence And Mortality ◽  
Echocardiographic Parameters ◽  
Post Hoc

Abstract Background Mitochondrial DNA (mtDNA) is a critical activator of inflammation. Circulating mtDNA released causes lung injury in experimental models. We hypothesized that elevated plasma mtDNA levels are associated with acute lung injury (ALI) in septic patients. Methods We enrolled 66 patients with sepsis admitted to the Department of Critical Care Medicine of Peking Union Medical College Hospital between January 2019 and October 2019. Respiratory, hemodynamic and bedside echocardiographic parameters were recorded. Plasma mtDNA, procalcitonin, interleukin 6, and interleukin 8 levels were examined. Results Plasma mtDNA levels within 24 h after admission were significantly increased in the group of septic patients with ALI [5.01 (3.38–6.64) vs 4.13 (3.20–5.07) log copies/µL, p 0.0172]. mtDNA levels were independently associated with mortality (hazard ratio, 3.2052; 95% CI 1.1608–8.8500; p 0.0253) and ALI risk (odds ratio 2.7506; 95% CI 1.1647–6.4959; p 0.0210). Patients with high mtDNA levels had worse outcomes, and post hoc tests showed significant differences in 28-day survival rates. Increased mtDNA levels were seen in patients with abdominal infection. Conclusions Increased plasma mtDNA levels within 24 h after admission were significantly associated with ALI incidence and mortality in septic patients.

scholarly journals A simple classification model for hospital mortality in patients with acute lung injury managed with lung protective ventilation*

2011 ◽  
Vol 39 (12) ◽  
pp. 2645-2651 ◽  
Author(s):  
Lisa M. Brown ◽  
Carolyn S. Calfee ◽  
Michael A. Matthay ◽  
Roy G. Brower ◽  
B. Taylor Thompson ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Hospital Mortality ◽  
Protective Ventilation ◽  
Classification Model ◽  
Lung Protective Ventilation ◽  
Simple Classification

Transient hemodynamic effects of recruitment maneuvers in three experimental models of acute lung injury*

2004 ◽  
Vol 32 (12) ◽  
pp. 2378-2384 ◽  
Author(s):  
Sung-Chul Lim ◽  
Alexander B. Adams ◽  
Dana A. Simonson ◽  
David J. Dries ◽  
Alain F. Broccard ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Experimental Models ◽  
Hemodynamic Effects ◽  
Recruitment Maneuvers

Recruitment Maneuvers in Three Experimental Models of Acute Lung Injury

2000 ◽  
Vol 161 (5) ◽  
pp. 1485-1494 ◽  
Author(s):  
THOMAS E.VAN der KLOOT ◽  
LLUIS BLANCH ◽  
A. MELYNNE YOUNGBLOOD ◽  
CRAIG WEINERT ◽  
ALEX B. ADAMS ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Experimental Models ◽  
Recruitment Maneuvers

Effect of eicosanoid inhibition on the development of pulmonary edema after acute lung injury

1996 ◽  
Vol 80 (3) ◽  
pp. 915-923 ◽  
Author(s):  
D. P. Schuster ◽  
A. H. Stephenson ◽  
S. Holmberg ◽  
P. Sandiford
Keyword(s):  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Experimental Models ◽  
Nuclear Medicine Imaging ◽  
Lung Water ◽  
Edema Formation ◽  
Cyclooxygenase Inhibition ◽  
Positron Emission

In experimental models of acute lung injury, cyclooxygenase inhibition improves oxygenation, presumably by causing a redistribution of blood flow away from edematous lung regions. This effect on perfusion pattern could also reduce alveolar edema formation. On the other hand, pulmonary pressures usually increase after cyclooxygenase inhibition, an effect that could exacerbate edema accumulation. Therefore we tested the following hypothesis: the total accumulation of pulmonary edema in dogs during a 24- to 28-h period of observation after acute lung injury caused by oleic acid will be less in a group of animals treated with meclofenamate (n = 6) or with the thromboxane-receptor blocker ONO-3708 (n = 5) than in a group of animals treated with oleic acid alone (placebo, n = 6). Lung water concentrations (LWC), the regional pattern of pulmonary perfusion, and protein permeability were measured with the nuclear medicine imaging technique of positron emission tomography. After 24-28 h, LWC was significantly less (P < 0.05) in the ONO-3708 group than in the meclofenamate group (a similar trend was seen compared with the placebo group, P = 0.12). After 24-28 h, pulmonary arterial pressures were highest in the meclofenamate group. Regardless of group, the only significant correlation with the change in LWC was with the integral of pulmonary pressures over the 24- to 28-h period. The data suggest that thromboxane inhibition will reduce edema accumulation in acute lung injury but that this effect depends on reducing as much as possible the simultaneous development of pulmonary hypertension from other causes.

scholarly journals Risk factors for underuse of lung-protective ventilation in acute lung injury

2012 ◽  
Vol 27 (3) ◽  
pp. 323.e1-323.e9 ◽  
Author(s):  
Allan J. Walkey ◽  
Renda Soylemez Wiener
Keyword(s):  
Risk Factors ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Protective Ventilation ◽  
Lung Protective Ventilation

Altered Levels of Trace Elements in Acute Lung Injury After Severe Trauma

2011 ◽  
Vol 147 (1-3) ◽  
pp. 28-35 ◽  
Author(s):  
Guanghuan Wang ◽  
Xiaoping Lai ◽  
Xiaojun Yu ◽  
Dian Wang ◽  
Xiaohu Xu
Keyword(s):  
Trace Elements ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Severe Trauma
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